[box type=”download”] Electrical basis of cardiac contractility Resting potential of myocytes and the trigger point for threshold Function of fast Na channels and Ca channels in shaping the cardiac action potential [/box]
Cardiac muscle electrophysiology
The resting potential of ventricular myocytes is approx..−90 mV (close to EK) and stable (phase 4).
An action potential is initiated when a threshold potential of approximately −65 mV is reached, as a result of transmission from an adjacent myocyte via gap junctions.
Fast, voltage-gated Na+ channels are activated, leading to an inward current which rapidly depolarizes the membrane towards +30 mV (phase 0).
The Na+ current rapidly inactivates, but, the initial depolarization activates voltage-gated Ca2+ channels (L-type channels; threshold approximately −45 mV), through which Ca2+ floods into the cell.
The resultant inward current prevents the cell from repolarizing, and causes a plateau phase (phase 2) that is maintained for ∼250 ms until the L-type channels inactivate.
The cardiac AP is thus much longer than that in nerve or skeletal muscle (∼300 ms vs ∼2 ms).
Repolarization is facilitated by activation of voltage-gated delayed rectifier K+ channels (phase 3).
The plateau and associated Ca2+ entry are essential for contraction; blockade of L-type channels (e.g. dihydropyridines) reduces force.
As the AP lasts almost as long as contraction, its refractory period prevents another AP being
initiated until the muscle relaxes; thus cardiac muscle cannot exhibit tetanus.